SLC12A2 Peptide
- Known as:
- SLC12A2 Peptide
- Catalog number:
- 42-498p
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- SLC12A2 Peptide
Related genes to: SLC12A2 Peptide
- Gene:
- SLC12A2 NIH gene
- Name:
- solute carrier family 12 member 2
- Previous symbol:
- -
- Synonyms:
- NKCC1, BSC, BSC2, PPP1R141
- Chromosome:
- 5q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-16
- Date modifiied:
- 2016-02-17
Related products to: SLC12A2 Peptide
Related articles to: SLC12A2 Peptide
- Venous thromboembolism (VTE) includes deep vein thrombosis (DVT) and pulmonary embolism (PE), which often originate from DVT and can be fatal. - Source: PubMed
Publication date: 2026/07/27
Lozano-Esparza SusanaShakt Gabrielle EBrody Jennifer AMartinez-Perez AngelConomos Matthew PGermain MarineClapham Katharine RTeder-Laving Marisvan Hylckama Vlieg AstridKauko AnniThibord FlorianBezerra Ohanna C LNadkarni GirishMunsch GaëlleNøst Therese HaugdahlGoode Ellen LJi YuekaiChasman Daniel IReiner Alexander PTurman ConstanceWiggins Kerri LSitlani Colleen MSouto Juan CarlosLutsey Pamela LBellomo TiffanyBiobank EstonianProgram Million VeteranLi-Gao RuifangWinstén Aleksi KristianFinnGen Chen Ming-HueiDo RonGourhant LénaickHveem KristianArmasu Sebastian MSaut NoémiePankratz NathanGiulianini FrancoHaessler JeffreySong MingyangOlaso RobertBoerwinkle EricDochtermann DanielSoria Jose ManuelRich Stephen SSmadja DavidKoyama SatoshiRosendaal Frits RNiiranen TeemuGagnon FranceMy T Vy HaZakai NeilLemarie CatherineSkogholt Anne HeidiDeleuze Jean-FrançoisPankow James SRidker Paul MLiu YuxiRice Ken MPyarajan SaijuCushman MaryEmmerich JospehPsaty Bruce MNatarajan PradeepJohnson Andrew DRodger Marc ASuchon PierreCouturaud FrancisMorange Pierre-EmmanuelTang WeihongKooperberg CharlesKabrhel ChristopherSabater-Lleal MariaTrégouët David-AlexandreWolberg Alisa SDamrauer Scott MSmith Nicholas L - Prenatal ethanol (alcohol) exposure (PreEE) results in abnormal tangential migration of medial ganglionic eminence (MGE)-derived GABAergic interneurons (GINs) in the embryonic mouse medial prefrontal cortex (mPFC); later in life, this is associated with impaired behavioral flexibility commonly seen in fetal alcohol spectrum disorders (FASD). The PreEE-induced abnormal tangential migration involves, in part, ethanol potentiating GABA receptor-mediated depolarization, the latter due to elevated intracellular chloride sustained primarily by the Na-K-Cl cotransporter NKCC1 in embryonic GINs. We previously reported that coincident administration of the NKCC1 antagonist bumetanide with PreEE prevents the PreEE-induced aberrant migration of GINs in the mPFC. However, such simultaneous dispensing rarely occurs in real life. In this light, the present study assessed whether bumetanide administered after PreEE mitigates the PreEE-induced aberrant tangential migration. - Source: PubMed
Koc BetulSkorput Alexander G JYeh Pamela W LYeh Hermes H - During early postnatal development, γ-aminobutyric acid (GABA) signaling undergoes a functional switch from excitation to inhibition, driven by age-dependent shifts in intracellular chloride concentrations ([Cl⁻]). In the retina, starburst amacrine cells (SACs) are pivotal for establishing direction-selective circuitry. However, the molecular mechanisms and the precise timing of the reversal potential of GABA-induced currents (E) shift in mouse SACs remain to be fully elucidated. We investigated the maturation of GABA responsiveness and chloride homeostasis in mouse SACs during the neonatal period. Ca imaging in dissociated retinal neurons revealed that the application of GABA markedly increased intracellular Ca concentrations in SACs on postnatal day (P) 0-P2, whereas these excitatory responses were largely absent by P7-P9. Gramicidin-perforated patch recordings showed that E underwent a significant hyperpolarizing shift with development, accompanied by a marked decrease in [Cl⁻]. Immunohistochemical analyses demonstrated a developmental decline in Na-K-2Cl⁻ co-transporter (NKCC1) expression and the concomitant up-regulation of K-Cl⁻ co-transporter (KCC2) in SACs. Consistent with these expression patterns, the pharmacological inhibition of NKCC1 or KCC2 selectively changed E in a stage-dependent manner. Collectively, these results demonstrate a developmentally regulated GABAergic switch in SACs orchestrated by coordinated changes in chloride transporter expression, providing insights into the physiological maturation of the retinal circuitry underlying direction selectivity. - Source: PubMed
Publication date: 2026/07/03
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Apablaza TábataVillanueva SandraOlave-Ruiz AraceliGuequen AnitaCatalán Marcelo AFlores Carlos A - Abdominal pain is a hallmark symptom of both inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS) and substantially impairs patients' quality of life. Relaxation response-based mind-body intervention (RR-MBI) has been reported to improve disease-specific outcomes and pain catastrophizing in both disorders, accompanied by whole-blood transcriptomic changes. However, the transcriptional features potentially relevant to abdominal pain before and after RR-MBI in IBS and IBD remain insufficiently explored. In this context, this study aimed to analyze these transcriptional changes and prioritize putative abdominal pain-relevant candidate genes from exploratory differentially expressed gene (DEG) sets. - Source: PubMed
Publication date: 2026/06/10
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